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Glucocorticoid- and Pioglitazone-Induced Proteinuria Reduction in Experimental Nephrotic Syndrome Both Correlate with Glomerular ECM Modulation

ABSTRACT: Glucocorticoid- and Pioglitazone-Induced Proteinuria Reduction in Experimental Nephrotic Syndrome Both Correlate with Glomerular ECM Modulation

PROVIDER: PRJNA1041459 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26855603_1.fastq.gz	Fastqsanger.gz
	SRR26855603_2.fastq.gz	Fastqsanger.gz
	SRR26855604_1.fastq.gz	Fastqsanger.gz
	SRR26855604_2.fastq.gz	Fastqsanger.gz
	SRR26855605_1.fastq.gz	Fastqsanger.gz

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Glucocorticoid- and Pioglitazone-Induced Proteinuria Reduction in Experimental Nephrotic Syndrome Both Correlate with Glomerular ECM Modulation

Project description:Idiopathic nephrotic Syndrome (NS) is a common glomerular disease. While glucocorticoids (GC) are the primary treatment, the PPARγ agonist pioglitazone (Pio) also reduces proteinuria in patients with NS and directly protects podocytes from injury. Since both drugs reduce proteinuria, we hypothesized these effects result from overlapping transcriptional patterns. Systems biology approaches compared glomerular transcriptomes from rats with PAN-induced NS treated with GC vs. Pio and identified 29 commonly regulated genes-of-interest, primarily involved in extracellular matrix (ECM) remodeling. Correlation with clinical idiopathic NS patient datasets confirmed glomerular ECM dysregulation as a potential mechanism of injury. Cellular deconvolution in silico revealed GC- and Pio-induced amelioration of altered genes primarily within podocytes and mesangial cells. While validation studies are indicated, these analyses identified molecular pathways involved in the early stages of NS (prior to scarring) suggesting that targeting glomerular ECM dysregulation may enable a future non-immunosuppressive approach for proteinuria reduction in idiopathic NS.

2024-12-01 | GSE248053 | GEO

Glucocorticoid- and pioglitazone-induced proteinuria reduction in experimental NS both correlate with glomerular ECM modulation.

Project description:Idiopathic nephrotic syndrome (NS) is a common glomerular disease. Although glucocorticoids (GC) are the primary treatment, the PPARγ agonist pioglitazone (Pio) also reduces proteinuria in patients with NS and directly protects podocytes from injury. Because both drugs reduce proteinuria, we hypothesized these effects result from overlapping transcriptional patterns. Systems biology approaches compared glomerular transcriptomes from rats with PAN-induced NS treated with GC vs. Pio and identified 29 commonly regulated genes-of-interest, primarily involved in extracellular matrix (ECM) remodeling. Correlation with clinical idiopathic NS patient datasets confirmed glomerular ECM dysregulation as a potential mechanism of injury. Cellular deconvolution in silico revealed GC- and Pio-induced amelioration of altered genes primarily within podocytes and mesangial cells. While validation studies are indicated, these analyses identified molecular pathways involved in the early stages of NS (prior to scarring), suggesting that targeting glomerular ECM dysregulation may enable a future non-immunosuppressive approach for proteinuria reduction in idiopathic NS.

| S-EPMC10770536 | biostudies-literature

Glomerular voom-transformed RNAseq counts from the Neptune Cohort and healthy living donors [re-analysis of GSE197307]

Project description:Glomerular Transcriptome in the Nephrotic Syndrome study network cohort

2024-02-07 | GSE254957 | GEO

Transcriptome profile of leukocyte RNA from children with steroid sensitive and resistant nephrotic syndrome

Project description:Glucocorticoid resistance complicates the treatment of ~20% of children with nephrotic syndrome, yet the molecular basis for resistance remains unclear. We generated the transcriptome profile by RNA sequencing of peripheral blood leukocytes from children obtained both at initial nephrotic syndrome presentation and after ~7 weeks of glucocorticoid therapy to identify genes or a gene panel able to differentiate steroid sensitive from steroid resistant nephrotic syndrome. RNA -seq analysis was followed by in-silico algorithm-based approaches and subsequent biochemical analyses on relevant candidate gene with important roles in podocyte and glomerular pathophysiology, using both patient samples and experimental models of nephrotic syndrome and podocyte injury.

2021-02-16 | GSE145969 | GEO

Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists

Project description:Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists

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RNAseq analysis of glomerular transcriptome of wild-type vs. Podocyte Cosmc knockout

Project description:Cosmc is an obligate chaperone for C1GalT1 T transferase necessary for generating mature mucin-type O-glycans. Animals lacking Cosmc in glomerular podocytes develop proteinuria, glomerulosclerosis and progressive renal failure. This study was designed to examine transcriptome differences in 1 month male animals with and without podocyte Cosmc, a time point when proteinuria is established but glomerular architecture is still relatively intact.

2019-03-04 | GSE126217 | GEO

Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists

Project description:Nephropathy was induced with puromycin amino-nucleoside (PAN) in Wistar rats and treated with daily treatments of Pioglitazone (Pio) and GQ-16. Total glomerular RNA was isolated, and mRNA libraries were generated and subjected to sequencing using NovaSeq6000 SP. Injury with PAN resulted in 1089 DEGs compared to controls, and 26 of these DEGs were restored by both Pio and GQ-16 treatments, whereas 106 unique GQ-16 regulated DEGs and 17 unique Pio-regulated DEGs were identified (Fig. 4A). Overall, Pio and GQ-16 treatment resulted in 75 and 173 DEGs compared to PAN injury, which included 29 common and 190 distinct genes (Fig. 4A). Of the 29 common DEGs, 28 DEGs were down-regulated by both Pio and GQ-16 and only 1 DEG upregulated by both treatments, when compared to PAN (Fig. 4B). Of the 190 distinct DEGs identified between Pio and GQ-16 treatments, 41 were down-regulated and 5 up-regulated by Pio and 124 down-regulated and 20 up-regulated by GQ-16 treatment.

2022-03-09 | GSE179945 | GEO

Spatiotemporal landscape of kidney tubular responses to glomerular proteinuria

Project description:Spatiotemporal landscape of kidney tubular responses to glomerular proteinuria

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Shared molecular targets in the glomerular transcriptome from patients with nephrotic syndrome and ANCA-associated vasculitis

Project description:Glomerular transcriptome from human kidney biopsies in Neptune and ERCB. A subset of samples profiled in this analysis were also profiled in Series GSE68127, and in GSE104066. Corresponding tubulointerstitial transcriptome data is submitted under GEO ID: GSE108113. RNA from the glomerular compartment was extracted and processed for hybridization on Affymetrix ST 2.1 microarrays, annotated using Human Entrez Gene ID custom CDF version 19. This dataset is part of the TransQST collection.

2018-05-17 | E-GEOD-108109 | biostudies-arrayexpress

LC MS/MS of calcium-sensing receptor (CaSR) knockdown in cultured murine podocytes versus wildtype

Project description:Calcimimetic agents allosterically increase the calcium (Ca2+) sensitivity of the calcium-sensing receptor (CaSR), which is expressed in the tubular system and to a lesser extent in podocytes. Activation of this receptor can reduce glomerular proteinuria and structural damage in proteinuric animal models. However, the precise role of the podocyte CaSR is still unclear. A CaSR knockdown in cultured murine podocytes and a podocyte-specific CaSR knockout in BALB/c mice were generated to study its role in proteinuria and kidney function. Podocyte CaSR knockdown abolished the calcimimetic R-568 mediated Ca2+-influx, disrupted the actin cytoskeleton, reduced cellular attachment and migration velocity. Adriamycin (ADR)-induced proteinuria enhanced glomerular CaSR expression in wild type mice. Albuminuria, podocyte foot process effacement, podocyte loss and glomerular sclerosis were significantly more pronounced in ADR-treated podocyte-specific CaSR knockout mice compared to wild type littermates. The co-treatment of WT mice with ADR and the calcimimetic cinacalcet reduced the proteinuria in WT, but not in podocyte specific CaSR knockout mice. In addition, four children with nephrotic syndrome, objecting glucocorticoid therapy, were treated with cinacalcet for 1 to 33 days. Proteinuria declined transiently by up to 96% and edema resolved. The activation of podocyte CaSR regulates key podocyte functions in vitro and reduces toxin induced proteinuria and glomerular damage in mice. Our findings suggest a potential novel role of CaSR signaling in control of glomerular disease. Proteomic samples: two backgrounds (CaSR Knockdown vs WT) two conditions (Treatment = 1µM R568 vs untreated control) two timepoints (24h and 48h) five replicates each 2 x 2 x 2 x 5 = 40 samples

2022-03-14 | PXD030416 | Pride

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